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Proceedings Paper

Effect of the prosurvival protein MCL-1 on photodynamic therapy induced apoptosis
Author(s): Jiaxing Song; Yunlong Li; Yanchun Wei
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Paper Abstract

Photodynamic Therapy (PDT), a promising and approved therapeutics for neoplastic and vascular disease, could induce expression of angiogenic and survival molecules including vascular endothelial growth factor, cyclooxygenase-2 (COX-2), and MCL-1. However, the precise effect of MCL-1 which is a member of the bcl-2 family on PDT is not well characterized. The work described here was aimed at determining whether expression of MCL-1 could exhibit a side effect on PDT. The results showed that expression of MCL-1 was increased prominently after Hela cells treated with PDT. By using confocal fluorescence microscopy and cell viability assay, it was found that overexpression of MCL-1 could have a vital influence on Photofrin-PDT-mediated apoptosis. Moreover, further analyses indicated that MCL-1 delayed translocation of Bax and release of cytochrome c from mitochrondria, further leading to cause a delay in cell apoptosis in Hela cells treated with PDT. The process was associated with MCL-1 interaction directly with Bax. In conclusion, overexpression of MCL-1 plays an important part in efficiency of PDT killing tumor cells, in other words, MCL-1 overexpression decreases PDT induced apoptosis through directly interacting with Bax. These results suggest that targeting MCL-1 expression might be a highly effective therapeutic measure for promoting the tumoricidal effectiveness of PDT.

Paper Details

Date Published: 6 March 2009
PDF: 10 pages
Proc. SPIE 7280, Seventh International Conference on Photonics and Imaging in Biology and Medicine, 72801T (6 March 2009); doi: 10.1117/12.822047
Show Author Affiliations
Jiaxing Song, South China Normal Univ. (China)
Yunlong Li, South China Normal Univ. (China)
Yanchun Wei, South China Normal Univ. (China)

Published in SPIE Proceedings Vol. 7280:
Seventh International Conference on Photonics and Imaging in Biology and Medicine
Qingming Luo; Lihong V. Wang; Valery V. Tuchin, Editor(s)

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